PTH has multiple, powerful effects on bone but it's anabolic actions are poorly understood. In animals, intermittent PTH administration increases both cortical and trabexular bone mass and can prevent, or even reverse, bone loss. In elderly people with osteoporosis, intermittent PTH administration increases trabecular bone mass but may accelerate cortical bone loss. In young women made acutely estrogen deficient, PTH increases bone mineral density (BMD) in trabecular-rich sites with no clear effect on cortical bone. In this proposal we will examine the effects of long-term, intermittent PTH administration on bone mass and bone turnover in early menopausal women with normal BMD. We will evaluate the effects of PTH on both cortical and trabecular BMD, assess the importance of aging and/or prior bone loss on the skeletal response to PTH, and attempt to identify markers that perdict the skeletal response to PTH, and attempt to identify markers that perdict the skeletal response to PTH and may suggest underlying mechanisms. Our model of early monopausal women with osteoporosis so that studies of PTH in this group are more likely to have detecable and interpretable results. Furthermore, this model eliminates prior bone loss as a factor in the skelatal response to PTH.